ArticlePediatric research2026
Bronchopulmonary dysplasia induced by hyperoxia attenuated by A GLP-1 analog, Liraglutide, by regulating the ACE-2/Ang(1-7)/Mas receptor pathway.
Article in Pediatric research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundGlucagon-like peptide-1 (GLP-1) shows promise for treating hyperoxia-induced bronchopulmonary dysplasia (BPD), but its mechanisms remain unclear. This study investigated the effects and potential mechanisms of GLP-1 using a hyperoxia-induced neonatal BPD mouse model.
methodsSprague-Dawley (SD) newborn rats were randomly assigned to four groups: control, hyperoxia, hyperoxia+Liraglutide, and hyperoxia+Liraglutide+A779. Lung tissues and bronchoalveolar lavage fluid (BALF) were collected at 3, 7, and 14 days post-exposure to air or hyperoxia. Hyperoxia-induced effects on lung development were assessed using haematoxylin and eosin staining. IL-6, TNF-α, and IL-1β levels in BALF were measured by ELISA. Expression of the ACE/AngII/AT1R and ACE-2/Ang(1-7)/Mas axes was analysed via reverse transcription-quantitative polymerase chain reaction (RT-qPCR), Western blotting, and immunohistochemistry.
resultsHyperoxia-induced BPD rats exhibited abnormal alveolar structure, characterized by simplified architecture, thickened septa, and a dysregulated renin-angiotensin system (RAS). Liraglutide significantly reduced hyperoxia-induced levels of IL-1β, TNF-α, and IL-6 in BALF and improved alveolar architecture. Moreover, when comparing the BPD group with the BPD+Lira+A779 group, the BPD+Lira group showed a notable decrease in relative mRNA expression of ACE, AngII, and AT1R (P < 0.05), while mRNA levels of ACE-2 and Ang1 increased significantly (P < 0.05). Consistent with RT-PCR findings, western blot analysis demonstrated that, in the BPD+Lira group, protein levels of ACE and AngII in the lung tissue of neonatal rats significantly lower in the BPD + Liraglutide group at postnatal days 3, 7, and 14 compared to both the BPD and BPD+Liraglutide+A779 groups. Conversely, ACE-2 and Ang(1-7) protein concentrations were markedly elevated. These results suggested that liraglutide may protect against hyperoxia-induced neonatal BPD by suppressing the ACE/AngII/AT1R axis and activating ACE-2/Ang(1-7)/Mas axis, an effect antagonized by A779.
conclusionsThese findings elucidated a mechanism whereby GLP-1 mitigated hyperoxia-induced BPD through inhibition of the ACE/AngII/AT1R pathway and activation of the ACE-2/Ang(1-7)/Mas axis. IMPACT: Liraglutide is capable to protect against hyperoxia-induced neonatal BPD in vitro. Liraglutide mitigated hyperoxia-induced BPD through inhibition of ACE/AngII/AT1R and activation of the ACE-2/Ang(1-7)/Mas axis. The ACE/AngII/AT1R and ACE-2/Ang(1-7)/Mas pathways could be one of those novel mechanisms for treating BPD.
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